Oxido nítrico renal en ratas espontáneamente hipertensas. Efecto de la angiotensina II

RISSO PATRON FACUNDO; MARAÑON RODRIGO; JOO TURONI CLAUDIO; BARRANCO CARLOS; PERAL DE BRUNO MARIA

Tafí del Valle - Tucumán

Jornada; XX Jornadas Científicas de la Asociación de Biología de Tucumán; 2003

Sociedad Tucumana de Biologia

The kidney is involved in the regulation of arterial pressure. In this mechanism interact different factors like nitric oxide(NO) which is a vasodilator agent presenting a greater reactivity in renal vessels. Alterations in the basal release of NO have been demonstrated in arterial hypertension(HTA). Likewise, angiotensin II(Ang II) in normal conditions induce NO release. The role of this hormone in the renal release of NO in models of HTA is not clear. OBJECTIVES:  To study  basal NO  release and stimulated release by Ang II in renal cortex of spontaneous hypertensive rats (SHR) METHODOLOGY:  Control rats Wistar (WK) and SHR were studied. Mean arterial pressure (MAP) was determined by a direct method. Several fractions of tissues were obtained (x=22.6±2.6 mg weight) of each renal cortex. NO content was measured by the Griess method. NO release was studied in different conditions: 1) during a period of equilibration without hormonal stimulation, with measurements each 20 minutes of washing; 2) in presence of different  concentrations of Ang II (10-8, 10-7 y 10-6 M); 3) in presence of L-NAME 10-4 M;  4) in presence of dexamethasone 10-4M (D). RESULTS: MAP values in SHR were increased (185.7±12 mmHg, n=6) in relation with WK (112±7.1 mmHg, n=7). SHR presented higher levels of  NO at 20 min of equilibration with regard to WK (32.5±10.3; n=27 vs. 6.9±2.2 nmoles /mg tissue, n=21, respectively, p<0.01). An effect of washing in SHR and in WK with stabilization at 40 minutes was found. Ang II (in all doses) increased significantly (p<0.05) NO in SHR and  WK with regard to basal levels without differences in the magnitude of both responses. In SHR and in WK neither L-NAME nor D modified NO basal levels. CONCLUSIONS: The finding that basal NO contents are higher in the renal cortex of SHR would indicate a contraregulator effect of NO in the intravascular renal  pressure increase. Similar values in the magnitude of the response to Ang II in the stimulated release of NO in SHR y WK would be explained by the already increased NO basal levels in SHR, as a consequence of the renal vascular hypertension of the model. In normotension these mechanisms would not be present  and would appear only in the response to the hypertensive agent Ang II. Absence of an effect of L-NAME in basal levels has been observed by other authors in isolated vascular tissues  and it could be due to increased endogenous L-Arginine levels. Results obtained with D discard that the increased NO in the renal cortex would be associated with an inflammatory reaction, indicating that in HTA SHR presents in their renal vessels an endothelial function preserved.